Effect of sex steroids on expression of sulfotransferase 2B1 immunoreactive protein in primary cultured porcine hepatocytes

Abstract

An excessive accumulation of androstenone (5α-androst-16-en-3-one) in pig adipose tissue is one of the two major contributors to the phenomenon of boar taint. High levels of adipose tissue androstenone have been related to a low rate of hepatic androstenone metabolism, which includes two stages: oxidative and conjugative. Sulfotransferases (SULTs), alongside with other specific enzymes, play the key role in the conjugative stage of androstenone metabolism. The present study investigated the mechanism regulating expression of sulfotransferase 2B1 (SULT2B1) immunoreactive protein using primary cultured pig hepatocytes as a model system. A specific objective was to determine whether the expression of pig hepatic SULT2B1 is regulated by the sex steroids; androstenone, testosterone and estrone sulphate. The study was performed on entire male pigs of a Large White (40%) × Landrace (40%) × Duroc (20%) cross-breed, average carcass weight 72.2 kg. The study shows that SULT2B1 immunoreactive protein expression can be induced by testosterone (final concentrations, 10 and 500 nM) and repressed by estrone sulphate (final concentration, 100 nM). Androstenone had no significant effect on SULT2B1 immunoreactive protein expression in the range of concentration, 10 nM to 1 μM. Time-courses (0 to 48 h) of steroid effects were investigated. The maximum effects of testosterone and estrone sulphate were observed in 24 h after the steroid treatments. This study provides direct evidence for involvement of sex steroids in the regulation of porcine hepatic SULTs.